Claudin 14/15 play important roles in early wallerian degeneration after rat sciatic nerve injury.
Claudin 14/15 play important roles in early wallerian degeneration after rat sciatic nerve injury.
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DOI：
10.1016/j.cjtee.2021.04.004
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发表时间：
2021-11
期刊：
影响因子：
--
通讯作者：
Yao DB
中科院分区：
文献类型：
--
作者：
Cai M;Shao J;Wang Y;Yung B;Li JN;Zhang HH;Li YT;Yao DB
沃勒氏变性（WD）是一种远端周围神经损伤的顺行变性过程。在这个过程中，许多基因受到不同的调控。然而，潜在的机制尚不清楚，特别是早期反应。我们旨在通过体内和体外cldn14 /15相互作用研究坐骨神经损伤对WD的影响。采用分子生物学和生物信息学分析的方法，研究了claudin 14/15参与WD的分子机制。我们之前的研究表明，claudins 14和claudins 15触发了受损坐骨神经的早期信号流和通路。在这里，我们报道了claudin 14和claudin 15之间的相互作用对早期WD神经变性和再生的影响。结果发现，WD患者坐骨神经中claudin 14/15表达上调。Claudin 14/15促进体外雪旺细胞增殖、迁移和抗凋亡。PKCα、NT3、NF2和bFGF在转染后的雪旺细胞中显著上调。此外，β-catenin、p-AKT/AKT、p-c-jun/c-jun和p-ERK/ERK信号通路的表达水平也显著改变。体外和体内实验中，Claudin 14/15通过β-catenin、p-AKT/AKT、p-c-jun/c-jun和p-ERK/ERK通路影响雪旺细胞增殖、迁移和抗凋亡。本研究结果可能有助于阐明周围神经退行性变的紧密连接信号通路的分子机制。
Wallerian degeneration (WD) is an antegrade degenerative process distal to peripheral nerve injury. Numerous genes are differentially regulated in response to the process. However, the underlying mechanism is unclear, especially the early response. We aimed at investigating the effects of sciatic nerve injury on WD via CLDN 14/15 interactions in vivo and in vitro. Using the methods of molecular biology and bioinformatics analysis, we investigated the molecular mechanism by which claudin 14/15 participate in WD. Our previous study showed that claudins 14 and 15 trigger the early signal flow and pathway in damaged sciatic nerves. Here, we report the effects of the interaction between claudin 14 and claudin 15 on nerve degeneration and regeneration during early WD. It was found that claudin 14/15 were upregulated in the sciatic nerve in WD. Claudin 14/15 promoted Schwann cell proliferation, migration and anti-apoptosis in vitro. PKCα, NT3, NF2, and bFGF were significantly upregulated in transfected Schwann cells. Moreover, the expression levels of the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK signaling pathways were also significantly altered. Claudin 14/15 affect Schwann cell proliferation, migration, and anti-apoptosis via the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK pathways in vitro and in vivo. The results of this study may help elucidate the molecular mechanisms of the tight junction signaling pathway underlying peripheral nerve degeneration.
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